Alcohol
Volume 26, Issue 2 , Pages 83-93, February 2002

Estradiol protects against cerebellar damage and motor deficit in ethanol-withdrawn rats☆

  • Marianna E Jung

      Affiliations

    • Department of Pharmacology and Neuroscience, University of North Texas HSC at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA
    • Corresponding Author InformationCorresponding author. Tel.: +1-817-735-0156; fax: +1-817-735-2091. E-mail address:(M.E. Jung)
    • ,
  • Shao H Yang

      Affiliations

    • Department of Pharmacology and Neuroscience, University of North Texas HSC at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA
    • ,
  • Anne-Marie Brun-Zinkernagel

      Affiliations

    • Department of Pathology and Anatomy, University of North Texas HSC at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA
    • ,
  • James W Simpkins

      Affiliations

    • Department of Pharmacology and Neuroscience, University of North Texas HSC at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA

Received 26 April 2001; received in revised form 18 October 2001; accepted 29 October 2001.

Abstract 

On the basis of findings obtained from this study, we hypothesize that the female sex steroid 17β-estradiol (E2) protects against cerebellar neuronal damage and behavioral deficit in rats withdrawn from chronic ethanol exposure. Ovariectomized rats implanted with E2 or an oil pellet received liquid ethanol (7.5% [wt./vol.]) or dextrin diet for 5 weeks, followed by 2 weeks of ethanol withdrawal. On termination of diet administration, rats were tested for both overt withdrawal signs and latency (seconds) to fall from an accelerating rotarod in six consecutive sessions (the longer the latency, the better the performance). The initial latency was measured separately to assess motoric capacity before learning occurred. Rats were then killed, and cerebella were prepared for accessing of Purkinje cell damage. The study revealed three specific findings. (1) In the absence of E2, the ethanol withdrawal group showed higher total ethanol withdrawal sign scores than those for the dextrin group, whereas the score for the ethanol withdrawal group was lower in the presence of E2. (2) In the absence of E2, the ethanol withdrawal group showed shorter rotarod latency than that for the dextrin group, whereas the latency for the ethanol withdrawal group increased in the E2-treated group. In ethanol withdrawal groups, E2 treatment also resulted in a longer latency than that observed with oil treatment in the initial session and in subsequent sessions. (3) Purkinje cell numbers in the ethanol withdrawal group without E2 were lower than those in dextrin groups and in the ethanol withdrawal group with E2 treatment. These findings support the suggestion that E2 exerts protective effects against withdrawal signs, cerebellar neuronal damage, and motoric impairment in subjects exposed to, and withdrawn from, chronic ethanol exposure.

Keywords:  17β-Estradiol, Neuroprotection, Chronic ethanol toxicity, Ethanol withdrawal, Cerebellum, Purkinje cells, Rotarod, Motor deficit

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

☆ Editor: T.R. Jerrells

PII: S0741-8329(01)00199-9

Alcohol
Volume 26, Issue 2 , Pages 83-93, February 2002

Article Tools

* Image Usage & Resolution